Detailed psychophysical analyses were performed of the abnormal pain sensations found in patients with reflex sympathetic dystrophy/causalgia. Touch-evoked pain (mechanical allodynia) was elicited by v. Frey hair stimuli that were near threshold for detection; on contralateral normal skin these same stimuli evoked innocuous tactile sensations. Transcutaneous electrical stimuli also evoked pain at intensities near threshold for detection; on normal skin these same stimuli evoke innocuous tactile sensations and activate A-beta low-threshold mechanoreceptors (A-beta-- LTMs). Reaction times for the painful sensation evoked by threshold-strength electrical stimuli were too fast to include a contribution from unmyelinated C-fiber nociceptive afferents. During an ischemic block, the pain evoked by threshold-strength v. Frey and electrical stimuli disappeared at the same time as impulse blockade in A- beta-LTMs; pain returned in concert with A-beta-LTM function. In these same patients, thresholds for heat-evoked pain and stimulus-response ratings for suprathreshold noxious heat stimuli were essentially normal; thus indicating that C-fiber nociceptors were not abnormally sensitized and did not contribute to the touch-evoked allodynia. These observations show that the touch-evoked pain of many RSD patients is due to an abnormality of CNS processing of input that normally evokes innocuous tactile sensations. In a subset of patients whose touch-evoked pain was otherwise conclusively shown to be A-beta-LTM dependent, ischemic block relieved the allodynia within 3-6 min., a time that is prior to any detectable impulse blockade in A- beta-LTMs. This observation indicates that a subset of patients have pain influenced by some aspect of circulatory occlusion other than its effect on impulse conduction. Lastly, we analyzed an advantageous case who had a focus of extremely painful sensibility that was separate from areas that supported mechanical allodynia of the A-beta-LTM dependent type. Infiltration of local anesthetic into the painful focus completely eliminated the patient's allodynia without any indication of anesthetic spreading to the previously symptomatic skin. The implication of this observation is that a focus of ongoing pain input dynamically maintains an abnormal CNS processor that is responsible for the "misread" of A-beta-LTM input.